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Psychoneuroendocrinology. 2019 Feb;100:32-40. doi: 10.1016/j.psyneuen.2018.09.024. Epub 2018 Sep 22.

Amygdalar activity predicts future incident diabetes independently of adiposity.

Author information

1
Cardiac MR-PET-CT Program, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA, 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St, MA, 02114, USA. Electronic address: mosborne@mgh.harvard.edu.
2
Cardiac MR-PET-CT Program, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA, 02114, USA. Electronic address: amorinaishai@gmail.com.
3
Cardiac MR-PET-CT Program, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA, 02114, USA. Electronic address: basmaabdelkader@gmail.com.
4
Cardiac MR-PET-CT Program, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA, 02114, USA. Electronic address: btung@nymc.edu.
5
Cardiac MR-PET-CT Program, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA, 02114, USA. Electronic address: ywang88@mgh.harvard.edu.
6
OMNI Biomarker Development, Genentech, Inc., 1 DNA Way, South San Francisco, CA, 94080, USA. Electronic address: baruch.amos@gene.com.
7
Translational and Molecular Imaging Institute, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Pl, New York, NY, 10029, USA. Electronic address: zahi.fayad@mssm.edu.
8
Department of Rheumatology, Columbia University, 630 W. 168th St, New York, NY, 10032, USA. Electronic address: jtg2122@cumc.columbia.edu.
9
Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit St, Boston, MA, 02114, USA. Electronic address: jlo@mgh.harvard.edu.
10
Department of Psychology, Tufts University, 490 Boston Ave, Medford, MA, 02155, USA; Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 149 13th St, Charlestown, MA, 02129, USA. Electronic address: Lisa.Shin@tufts.edu.
11
Neuroendocrine Unit, Massachusetts General Hospital, 55 Fruit St, Boston, MA, 02114, USA; Nutritional Metabolism, Massachusetts General Hospital, 55 Fruit St, Boston, MA, 02114, USA. Electronic address: sgrinspoon@mgh.harvard.edu.
12
Harvard University T.H. Chan School of Public Health, 677 Huntington Ave, Kresge Building, Boston, MA, 02115, USA. Electronic address: kkoenen@hsph.harvard.edu.
13
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 149 13th St, Charlestown, MA, 02129, USA. Electronic address: roger.pitman@mgh.harvard.edu.
14
Cardiac MR-PET-CT Program, Massachusetts General Hospital, 165 Cambridge St, Suite 400, Boston, MA, 02114, USA; Cardiology Division, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St, MA, 02114, USA. Electronic address: atawakol@mgh.harvard.edu.

Abstract

While it is established that psychosocial stress increases the risk of developing diabetes mellitus (DM), two key knowledge gaps remain: 1) the neurobiological mechanisms that are involved in mediating that risk, and 2) the role, if any, that adiposity plays in that mechanism. We tested the hypotheses that: 1) metabolic activity in the amygdala (AmygA), a key center involved in the neurobiological response to stress, associates with subsequent DM risk, and 2) this association is independent of adiposity. AmygA and adipose tissue volumes were measured, and serial blood assessments for DM were obtained in 232 subjects who underwent combined 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) imaging. Higher baseline AmygA predicted subsequent, new-onset DM, independently of adiposity and other DM risk factors. Furthermore, higher adiposity only increased DM risk in the presence of higher AmygA. In a separate cross-sectional cohort, higher AmygA associated with higher insulin resistance. Accordingly, the current study shows, for the first time, that activity in a stress-responsive neural region predicts the onset of DM. Further, we observed that this neurobiological activity acts independently of, but also synergistically with adiposity to increase DM risk. These findings suggest novel therapeutic targets to help manage and possibly prevent DM.

KEYWORDS:

Amygdala; Diabetes mellitus; Positron emission tomography/computed tomography; Visceral adiposity

PMID:
30273797
PMCID:
PMC6398601
[Available on 2020-02-01]
DOI:
10.1016/j.psyneuen.2018.09.024

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